In man, intravenous infusion of adenosine has been useful in inducing sustained hypotension during anesthesia. Bolus injections terminate supraventricular tachyarrhythmias by delaying AV node conduction. It has been proposed that some of its cardiovascular effects are related to inhibition of noradrenergic neurotransmission. We assessed the cardiovascular and sympathoadrenal effects of intravenous infusion of adenosine (10 to 140 micrograms/kg/min) in 7 conscious normal subjects. At the highest infusion rate achieved, adenosine increased heart rate by 33 bpm (p less than 0.005), increased systolic blood pressure by 13 mm Hg (p less than 0.02) and decreased diastolic blood pressure by 8 mm Hg (p less than 0.02). Plasma norepinephrine and epinephrine increased 44% and 213% respectively. Basal plasma renin activity was 0.7 +/- 0.09 ng AI/ml/hr and remained unchanged. Higher doses were not given due to the appearance of subjective side effects (headache, nervousness, flushing and an urge to breathe deeply). During dipyridamole administration, 4-fold lower doses were required to produce equivalent cardiovascular effects. We conclude that in conscious man, intravenous infusion of adenosine is associated with activation rather than inhibition of the sympathoadrenal system. The possible mechanisms of this sympathetic activation are discussed.